Download ADP-Ribosylation Reactions: From Bacterial Pathogenesis to by Felix R. Althaus, Hanna E. Kleczkowska (auth.), Rafael PDF

By Felix R. Althaus, Hanna E. Kleczkowska (auth.), Rafael Alvarez-Gonzalez (eds.)

This particular factor of Molecular and mobile Biochemistry comprises twenty-two chosen examine papers and reports from a complete of 1 hundred and ten shows given on the twelfth overseas Symposium on ADP-ribosylation Reactions: From Bacterial Pathogenesis to melanoma, held in Cancun, Mexico, might 10-14, 1997. The Symposium was once hosted by way of the Sociedad Mexicana de Bioquimica and used to be subsidized by way of the collage of North Texas future health technological know-how middle, fortress worthy, TX, united states.
This quantity offers a cutting-edge resource of data for simple scientists and clinicians who're drawn to the molecular, biochemical, and mobile facets of protein-(ADP-ribose) move reactions in human healthiness and disease.

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Extra resources for ADP-Ribosylation Reactions: From Bacterial Pathogenesis to Cancer

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Conversely, 39 GXXXXGKSIT t DXXG t NKXD t 29-QFPEVYVP 27-AFPGEYlP 27-KFPSEYVP 27-HFVDEYDP T T T T t * + RhoA Racl Cdc42 Ha-Ras SXK VFE VFD VFD lED N YVADlE-47 N YSANVM-45 N YAVTVM-45 S YRKQVV-45 Fig. 2. Structural domains within Rho GTPases. The domains involved in GTP-bindinglhydrolysis, prenylation, and effector interaction are highlighted. Clostridium botulinum exoenzyme C3 ADP-ribosylates Rho at Asn41 '*'), whereas Clostridium difficile toxins monoglucosylate Rho/Rac/ Cdc42 at Thr37 (or equivalent '+').

3, open symbols), there was a dose-dependent increase in the plasmid mutation frequency in both cell lines, as expected. Pretreatment of COM3 cells with 50 nM Dex (Fig. 3, filled square symbols), resulting in trans-dominant PARP inhibition [21], led to a significant potentiation of the mutation induction by MNU at all concentrations tested, but interestingly had no effect on mutation frequency in the absence ofMNU treatment. -~---1 o 10 20 30 40 MNU (mM) Fig. 2. Survival of MNU-treated shuttle vector directly transformed into E.

Mutation frequency ofMNU-treated shuttle vector passaged through COM3 or COR3 cells. COM3 cells, which overexpress the human PARP DNA-binding domain after induction with dexamethasone (Dex), and COR3 control cells were induced or not with Dex as indicated, followed by electroporation of plasmid p YZ289 that had been exposed to the indicated concentrations of MNU in vitro. Plasmid mutation frequencies were determined as described in Materials and methods and are plotted a as function of MNU concentration.

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